Cardiac troponin T in chest pain unit patients without ischemic electrocardiographic changes: angiographic correlates and long-term clinical outcomes

OBJECTIVES

We prospectively evaluated the relation between cardiac troponin T (cTnT) level, the presence and severity of coronary artery disease (CAD) and long-term prognosis in patients with chest pain but no ischemic electrocardiographic (ECG) changes who had short-term observation.

BACKGROUND

Cardiac TnT is a powerful predictor of future myocardial infarction (MI) and death in patients with ECG evidence of an acute coronary syndrome. However, for patients with chest pain with normal ECGs, it has not been determined whether cTnT elevation is predictive of CAD and a poor long-term prognosis.

METHODS

In 414 consecutive patients with no ischemic ECG changes who were triaged to a chest pain unit, cTnT and creatine kinase, MB fraction (CK-MB) were evaluated ≥10 h after symptom onset. Patients with adverse cardiac events, including death, MI, unstable angina and heart failure were followed for as long as one year.

RESULTS

A positive (>0.1 ng/ml) cTnT test was detected in 37 patients (8.9%). Coronary artery disease was found in 90% of 30 cTnT-positive patients versus 23% of 144 cTnT-negative patients who underwent angiography (p < 0.001), with multivessel disease in 63% versus 13% (p < 0.001). The cTnT-positive patients had a significantly (p < 0.05) higher percent diameter stenosis and a greater frequency of calcified, complex and occlusive lesions. Follow-up was available in 405 patients (98%). By one year, 59 patients (14.6%) had adverse cardiac events. The cumulative adverse event rate was 32.4% in cTnT-positive patients versus 12.8% in cTnT-negative patients (p = 0.001). After adjustment for baseline clinical characteristics, positive cTnT was a stronger predictor of events (chi-square = 23.56, p = 0.0003) than positive CK-MB (>5 ng/ml) (chi-square = 21.08, p = 0.0008). In a model including both biochemical markers, CK-MB added no predictive information as compared with cTnT alone (chi-square = 23.57, p = 0.0006).

CONCLUSIONS

In a group of patients with chest pain anticipated to have a low prevalence of CAD and a good prognosis, cTnT identifies a subgroup with a high prevalence of extensive and complex CAD and increased risk for long-term adverse outcomes.     

The use of human heart-type fatty acid-binding protein as an early diagnostic biochemical marker of myocardial necrosis in patients with acute coronary syndrome, and its comparison with troponin-T and creatine kinase–myocardial band

Heart-type fatty acid-binding protein (H-FABP), a new biochemical marker of sarcolemmal injury due to acute myocardial ischemia, can be used as a tool in early diagnosis and management of patients at high risk. The aim of this study was to determine the early diagnostic value of H-FABP in acute coronary syndrome (within 6–24 h of chest pain) and to compare it with troponin-T (TnT) and creatine kinase–myocardial band (CK-MB) for accuracy. The study consisted of 40 consecutive patients with chest pain admitted to the coronary care unit with the diagnosis of suspected acute coronary syndrome. The patient population consisted of two groups according to the time of admission; the first group (26 patients) included patients admitted within 6 h of chest pain, and the second group (14 patients) included patients admitted within 6–24 h of chest pain. The blood samples for H-FABP, TnT, and CK-MB were obtained at admittance, at the 6th, and at the 24th hours for the first group, and at admittance and at the 24th hours for the second. Statistical analysis was performed among the 26 patients for the first 6 h values, and among all 40 patients for the values obtained within 6–24 h and at the 24th hour. The patients were then divided into groups according to the changes in the electrocardiogram (ECG) and cardiac enzymes as unstable angina pectoris, non-ST elevation myocardial infarction (MI), and ST-elevation MI. Coronary angiography was performed in 38 (95%) patients. Sensitivity of TnT, CK-MB, and H-FABP in the first group (within 6 h of chest pain) were 38%, 76%, and 95% respectively. The sensitivity of H-FABP was significantly higher than TnT (P = 0.014). Sensitivity of TnT, CK-MB, and H-FABP tests in the second time period (within 6–24 h of chest pain) were 100%, 90%, and 91% respectively. In this time period, the sensitivity of TnT was higher than H-FABP, but it was statistically insignificant. At the 24th hour, sensitivity of TnT was 100%, CK-MB 90%, and H-FABP 27.3%, and TnT and CK-MB were more sensitive than H-FABP for the whole group (P = 0.002). In the first group (within 6 h of chest pain) H-FABP positivity was slightly but insignificantly higher in patients with two- and three-vessel disease compared with those with one-vessel disease (60.7% and 33.3%, P = 0.19) and in the same group, patients who underwent primary coronary intervention had a significantly higher H-FABP positivity than others (80%, 32%, P = 0.02). Within 6–24 h of chest pain, H-FABP positivity was 80% in patients with one-vessel disease and 71.4% in patients with two- and three-vessel disease (P = 0.69). Within 6–24 h, positivity of H-FABP reached a peak value of 100% in patients who underwent primary coronary intervention, while H-FABP was positive in 60% of the others (P < 0.001). We conclude that within the 6 h of acute coronary syndrome, H-FABP seems to be a more sensitive biochemical marker than TnT in the early detection of ischemic myocardial necrosis. But after the first 6 h of the onset of chest pain the sensitivity of H-FABP decreases, and this marker should not be used alone in patients admitted 24 h after the onset of chest pain.     

The predictive value of the bedside troponin T test for patients with acute chest pain

BACKGROUND: The evaluation of patients with acute chest pain is time consuming and complicated. In the present study, the role of the bedside troponin T (TnT) test was prospectively investigated for predicting the risk of death and acute heart failure (AHF) in patients with acute chest pain. METHODS: Five hundred two consecutive patients admitted in the 24 h after the onset of chest pain were enrolled in the study. Tests of bedside TnT, qualitative troponin I, myoglobin, creatine kinase and creatine kinase (muscle-brain), and electrocardiography were performed on these patients. RESULTS: For the bedside TnT test, 160 (31.9%) patients had positive results and 323 (64.3%) patients had negative results. During 30 days of follow-up, the differences between TnT-positive and TnT-negative patients were as follows: 139 (86.9%) positive patients and seven (2.2%) negative patients were diagnosed with acute myocardial infarction (AMI) (OR=298.8 for AMI in positive versus negative patients); 51 (31.9%) positive patients and 37 (11.5%) negative patients had AHF (OR=3.6 for AHF in positive versus negative patients); 39 (24.4%) positive patients and 15 (4.6%) negative patients died (OR=6.7 for all-cause death in positive versus negative patients); 31 (19.4%) positive patients and five (1.5%) negative patients died due to a cardiac event (OR=15.8 for cardiac death in positive versus negative patients). The sensitivity and specificity of the bedside TnT test for diagnosing AMI were 95.2% and 93.8%, respectively. CONCLUSIONS: The bedside TnT test is a powerful, independent and valuable tool for risk stratification in patients with acute chest pain.     

Ninety-minute accelerated critical pathway for chest pain evaluation

Rapid, efficient, and accurate evaluation of chest pain patients in the emergency department optimizes patient care from public health, economic, and liability perspectives. To evaluate the performance of an accelerated critical pathway for patients with suspected coronary ischemia that utilizes clinical history, electrocardiographic findings, and triple cardiac marker testing (cardiac troponin I [cTnI], myoglobin, and creatine kinase-MB [CK-MB]), we performed an observational study of a chest pain critical pathway in the setting of a large Emergency Department at the Veterans Affairs Medical Center in 1,285 consecutive patients with signs and symptoms of cardiac ischemia. The accelerated critical pathway for chest pain evaluation was analyzed for: (1) accuracy in triaging of patients within 90 minutes of presentation, (2) sensitivity, specificity, positive predictive value, and negative predictive value of cTnI, myoglobin, and CK-MB in diagnosing acute myocardial infarction (MI) within 90 minutes, and (3) impact on Coronary Care Unit (CCU) admissions. All MIs were diagnosed within 90 minutes of presentation (sensitivity 100%, specificity 94%, positive predictive value 47%, negative predictive value 100%). CCU admissions decreased by 40%. Ninety percent of patients with negative cardiac markers and a negative electrocardiogram at 90 minutes were discharged home with 1 patient returning with an MI (0.2%) within the next 30 days. Thus, a simple, inexpensive, yet aggressive critical pathway that utilizes high-risk features from clinical history, electrocardiographic changes, and rapid point-of-care testing of 3 cardiac markers allows for accurate triaging of chest pain patients within 90 minutes of presenting to the emergency department.     

Early positive biomarker in relation to myocardial necrosis and impaired fatty acid metabolism in patients presenting with acute chest pain at an emergency room.

BACKGROUND: Measurement of circulating biomarkers has enabled early diagnosis and risk assessment of acute coronary syndrome. This study sought diagnostic values of the first single-point data of biomarkers obtained soon after patient arrival by comparing with scintigraphically quantified myocardial injury in patients presenting with acute chest pain at an emergency room. METHODS AND RESULTS: Serial blood samples were taken soon after arrival in an emergency department in 74 patients with suspected acute coronary syndrome to quantify blood levels of troponin-T (TnT), heart-type fatty acid-binding protein (H-FABP), myocardial-bound creatine kinase (CK-MB), and myoglobin. Myocardial perfusion and metabolic defects were scintigraphically quantified. The first single-point data had high positive predictive values for detecting the defects (80-100%) but low negative predictive values (15-41%). CK-MB and TnT had higher specificities (73-100%) but significantly lower positive rates (22-27%) than the others (61-68%), resulting in greater sensitivities of H-FABP and myoglobin (75-80%) than those of CK-MB and TnT (29-35%). Among biomarkers, TnT peak concentrations most closely correlated with scintigraphic abnormalities. CONCLUSION: H-FABP can contribute to early detection of myocardial injury and TnT is most likely to correlate with injured myocardial mass. The differential features of biomarkers are complementary in patients with acute chest pain presenting at an emergency room.     

The prognostic significance of serial myoglobin,troponin I,and creatine kinase-MB measurements in patients evaluated in the emergency department for acute coronary syndrome

STUDY OBJECTIVE: We sought to determine the value of serial measurements of myoglobin, cardiac troponin I (cTnI), and creatine kinase-MB (CK-MB) to predict 30-day adverse events in patients evaluated in the emergency department (ED) for possible acute coronary syndrome. METHODS: Serum myoglobin, cTnI, and CK-MB levels were measured at presentation, 90 minutes, 3 hours, and 9 hours in patients evaluated in the ED for possible acute coronary syndrome. In 764 consecutive patients, the ability of each individual marker and combination of markers to predict a 30-day adverse event (death or myocardial infarction) over time was calculated. RESULTS: There were 109 (14%) patients with an adverse event at 30 days (84 myocardial infarctions and 43 deaths). The sensitivities of initial measurements of myoglobin, cTnI, and CK-MB for identifying adverse events were 60%, 47%, and 52%, respectively. The combined sensitivity of myoglobin and cTnI measurements during a 9-hour period was 94%; specificity was 50%. Measurement of CK-MB did not improve sensitivity. CONCLUSION: The measurement of both myoglobin and cTnI during a 9-hour period was the most predictive of subsequent adverse events in patients evaluated in the ED for possible acute coronary syndrome.     

A prospective study of an algorithm using cardiac troponin I and myoglobin as adjuncts in the diagnosis of acute myocardial infarction and intermediate coronary syndromes in a veteran's hospital

BACKGROUND: Accurate and cost-effective evaluation of acute chest pain has been problematic for years. The high prevalence of missed myocardial infarctions (MI) has led to conservative triage behavior on the part of physicians, leading to expensive admissions to coronary care units. New algorithms are sorely needed for more rapid and accurate triage of patients with chest pain to appropriate treatment settings. HYPOTHESIS: We sought to test an algorithm for rapid diagnosis of MI and acute coronary syndromes using cardiac troponin I (cTnI) and myoglobin as adjuncts to creatine kinase (CK)-MB. We hypothesized our algorithm would be both sensitive and specific at early time points, and would allow safe stratification of patients not ruling in by conventional CK-MB criteria. METHODS: This was a 6-month prospective study of 505 consecutive patients who presented with chest pain at a university-affiliated veteran's hospital. The percentage of MIs at various time points was identified using combinations of markers. Safety outcomes were assessed by follow-up of patients discharged home. Cost savings analysis was assessed by surveying the physicians as to whether the use of the algorithm affected their disposition of patients. Forty-nine patients ruled in for MI. Using the combination of cTnI, 2-h doubling of myoglobin, and CK-MB, 37 (76%) ruled in at the time of presentation, 43 (88%) at 2 h, and 100% by 6 h. RESULTS: Cardiac troponin I plus a 2-h myoglobin was as accurate as the combination of all three markers and performed better than CK-MB in detecting patients presenting late and as a predictor for complications when CK-MB was normal. Of the 456 patients with normal markers after 6 h, only 140 were sent to the coronary care unit (CCU), and 176 were sent home. A 3-month follow-up showed minimal adverse events. One-half of physicians completing a survey stated the use of markers changed their disposition of patients, leading to an estimated 6-month cost savings of a half-million dollars. CONCLUSIONS: We developed an algorithm using troponin I and myoglobin as adjuncts to usual CK-MB levels that allowed for rapid and accurate assessment of patients with acute MI. It also afforded physicians important input into their decision making as to how best to triage patients presenting with chest pain. Their comfort in sending home certain subgroups of patients who otherwise would have been admitted to the CCU was rewarded with a good short-term prognosis and a large cost savings to the hospital.     

Diagnostic marker cooperative study for the diagnosis of myocardial infarction

BACKGROUND: Millions of patients present annually with chest pain, but only 10% to 15% have myocardial infarction. Lack of diagnostic sensitivity and specificity of clinical and conventional markers prevents or delays treatment and leads to unnecessary costly admissions. Comparative data are lacking on the new markers, yet using all of them is inappropriate and expensive. METHODS AND RESULTS: The Diagnostic Marker Cooperative Study was a prospective, multicenter, double-blind study with consecutive enrollment of patients with chest pain presenting to the emergency department. Diagnostic sensitivity and specificity and frequency of increase in patients with unstable angina were determined for creatine kinase-MB (CK-MB) subforms, myoglobin, total CK-MB (activity and mass), and troponin T and I on the basis of frequent serial sampling for 相似文献   

Usefulness of myocardial necrosis triad markers for predicting 4-year mortality in patients with suspected acute coronary syndrome

OBJECTIVE: Cardiac troponins (cTn), creatine kinase-MB (CK-MB), myoglobin (MYO) are commonly used biochemical markers for risk stratification and diagnosis in patients with suspected acute coronary syndrome (ACS). The aim of the study was to analyse the prognostic implications of 3 myocardial necrosis markers measured at admission in the long-term observation. METHODS: The study group consisted of 336 consecutive patients whose concentration of cTnl, CK-MB and MYO were measured at admission. Patients were categorized into 4 groups according to the number of positive myocardial necrosis markers. RESULTS: There was a significant increase in the mean marker levels with increasing numbers of positive markers (over upper normal range): cTnl (0.02 +/- 0.06; 0.7 +/- 1.9; 3.4 +/- 8.8; 5.1 +/- 9.2 ng/ml; P < 0.001), CK-MB (1.3 +/- 1.1; 3.3 +/- 3.9; 21.9 +/- 39.4; 37.5 +/- 48.4 ng/ml; P < 0.001), MYO (39.4 +/- 16.5; 94.5 +/- 91; 202.2 +/- 172.2; 320.3 +/- 234.3 ng/ml; P < 0.001). There was a statistically significant increase in the 4-year all-cause mortality with increasing numbers of positive markers; P value for trend < 0.0001. CONCLUSIONS: All 3 marker levels at admission may be an important addition to the risk stratification of patients with suspected ACS and a potentially important target for therapy. They have prognostic implications in the long-term observation of patients with chest pain and suspected ACS.     

Prognostic value of troponin T, myoglobin, and CK-MB mass in patients presenting with chest pain without acute myocardial infarction.

OBJECTIVE: To assess the prognostic value of minor myocardial damage in patients presenting with chest pain without myocardial infarction. DESIGN: The relative risk of suffering a cardiac event in the next six months was assessed in patients with minor myocardial damage assessed by the cardiac markers CK-MB, myoglobin, and troponin T. SETTING: Emergency department of a large university hospital. PATIENTS: In 128 consecutive patients with chest pain, acute myocardial infarction (by WHO criteria) was ruled out; of these, 39 had a rise and fall of one or more markers, indicating minor myocardial damage. The presence of a documented history of coronary artery disease was assessed on admission. RESULTS: 24 patients had a subsequent event (cardiac death, acute myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting) in the next six months. An abnormal troponin T predicted a subsequent event while abnormal CK-MB or myoglobin did not. The relative risk for troponin T was 2.8 (95% confidence interval: 1.0 to 7.9), for myoglobin 1.0 (0.3 to 3.2), and for CK-MB 0.9 (0.2 to 3.4). A documented history of coronary artery disease predicted subsequent events with a relative risk of 3.9 (1.3 to 11.3). CONCLUSIONS: Troponin T was the only marker that predicted future events, but a documented history of coronary artery disease was the best predictor in patients in whom an acute myocardial infarction had been ruled out.     

A comparison of cardiac troponin T and creatine kinase-MB for patient evaluation after cardiac surgery

OBJECTIVES: The aim of this study was to assess the role of serum markers of myocardial necrosis after cardiac surgery. BACKGROUND: The role of serum troponin T (TnT) and creatine kinase-MB (CK-MB) for the risk stratification of patients after cardiac surgery remains undefined. METHODS: Serum levels of TnT and CK-MB were measured from 224 patients every 8 h after cardiac surgery. The results of serum cardiac marker testing were correlated with adverse events, including new myocardial infarction (MI), cardiogenic shock or death. Univariable analysis identified factors predictive of complications, while stepwise logistic regression identified independent predictors of postoperative complications. RESULTS: Cardiac marker elevation was universal after cardiac surgery. At all time points measured, compared with those patients without complications, the TnT levels from patients with complications were more significantly elevated (all: p < 0.0005). In contrast, among identically timed specimens, the levels of CK-MB from complicated patients were less reliably discriminatory. Multivariable analysis suggested that a TnT level in the highest quintile (> or = 1.58 ng/ml) was the strongest predictor of complications, including death (post-op, odds ratio [OR] = 31.0, 95% confidence interval [CI] = 3.67 to 263.1, p = 0.002) or shock (post-op: OR = 18.9, 95% CI = 2.29 to 156.1, p = 0.006; 18 h to 24 h: OR = 30.7, 95% CI = 3.75 to 250.7, p = 0.001), as well as the composite end points of death/MI (18 h to 24 h: OR = 60.1, 95% CI = 7.34 to 492.1, p < 0.0005), shock/MI (post-op: OR = 23.3, 95% CI = 2.82 to 191.4, p = 0.003; 18 h to 24 h: OR = 37.8, 95% CI = 4.66 to 307.3, p = 0.001) or death/shock/MI (post-op: OR = 20.0, 95% CI = 2.81 to 142.0, p = 0.003; 18 h to 24 h: OR = 67.4, 95% CI = 6.96 to 652.3, p < 0.0005). In contrast, in the presence of TnT, the results of CK-MB measurement added no independent prognostic information. CONCLUSIONS: Troponin T is superior to CK-MB for the prediction of impending complications after cardiac surgical procedures.     

Angiographic adverse events during percutaneous coronary intervention fail to predict creatine kinase-MB elevation.

We attempted to determine if aggressive detection of angiographic adverse events during coronary intervention could predict subsequent creatine kinase (CK)-MB elevations. During coronary intervention, both fluoroscopy and cine angiography were used to detect angiographic adverse events. At least one angiographic adverse event occurred in 133/251 (53%) of procedures. CK-MB elevation occurred in 24% of procedures. Slow flow during the procedure (P=0.002) and chest discomfort at the end of the procedure (P=0.007) were the strongest predictors of CK-MB elevation. Among procedures with no angiographic adverse events, CK-MB elevation occurred in 15/121 (12%), accounting for 25% of CK-MB elevations. We conclude that CK-MB elevation occurs after angiographically uncomplicated coronary interventions even when angiographic adverse events are aggressively detected. Routine monitoring of cardiac enzymes is necessary to detect all patients who will experience myocardial injury after coronary intervention.     

Evaluation of troponin T criteria for periprocedural myocardial infarction in patients with acute coronary syndromes

In patients with acute coronary syndromes undergoing percutaneous coronary intervention (PCI), the diagnosis of periprocedural myocardial infarction is often problematic when the pre-PCI levels of cardiac troponin T (TnT) are elevated. Thus, we examined different TnT criteria for periprocedural myocardial infarction when the pre-PCI TnT levels were elevated and also the associations between the post-PCI cardiac marker levels and outcomes. We established the relation between the post-PCI creatine kinase-MB (CKMB) and TnT levels in 582 patients (315 with acute coronary syndromes and 272 with stable coronary heart disease). A post-PCI increase in the CKMB levels to 14.7 μg/L (3 × the upper reference limit [URL] in men) corresponded to a TnT of 0.23 μg/L. In the 85 patients with acute coronary syndromes and normal CKMB, but elevated post peak TnT levels before PCI (performed at a median of 5 days, interquartile range 3 to 7), the post-PCI cardiac marker increases were as follows: 21 (24.7%) with a ≥ 20% increase in TnT, 10 (11.8%) with an CKMB level >3 × URL, and 12 (14%) with an absolute TnT increase of >0.09 μg/L (p <0.005 for both). In the patients with stable coronary heart disease and post-PCI cardiac markers > 3× URL compared to those without markers elevations, the rate of freedom from death or nonfatal myocardial infarction was 88% for those with TnT elevations versus 99% (p <0.001, log-rank) and 84% for those with CKMB elevations versus 98% (p <0.001, log-rank). Of the patients with acute coronary syndromes, the post-PCI marker levels did not influence the outcomes. In conclusion, in patients with acute coronary syndromes and elevated TnT levels undergoing PCI several days later, ≥20% increases in TnT were more common than absolute increments in the TnT or CKMB levels of >3× URL. Also, periprocedural cardiac marker elevations in patients with acute coronary syndromes did not have prognostic significance.     

Systemic inflammation in unstable angina is the result of myocardial necrosis

OBJECTIVES: We investigated whether the source of the acute phase response in unstable angina (UA) lay within the culprit coronary plaque or distal myocardium. BACKGROUND: An inflammatory response is an important component of the acute coronary syndromes. However, its origin and mechanism remain unclear. METHODS: In 94 stable patients undergoing coronary angiography, the relationship between systemic levels of tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6) and C-reactive protein (CRP) and extent of atherosclerosis was studied. The temporal relationship between these markers and troponin T (TnT) was determined in 91 patients with UA. Cytokine levels were measured in the aortic root and coronary sinus of 36 unstable patients. RESULTS: There was no relationship found between stable coronary atherosclerosis and inflammatory marker levels. Compared with this group, admission levels of IL-6 (3.6 +/- 0.3 ng/ml vs. 10.7 +/- 1.7 ng/ml, p < 0.05) and CRP (2.3 +/- 0.1 mg/l vs. 4.6 +/- 0.6 mg/l, p < 0.05) were elevated in patients with UA. In this group, IL-6 and CRP remained elevated in those who subsequently experienced major adverse cardiac events. This inflammatory response occurred in parallel to the appearance of TnT. Both TNF-alpha (19.2 +/- 3.4 ng/ml vs. 17.1 +/- 3.3 ng/ml, p < 0.001) and IL-6 (10.3 +/- 1.4 ng/ml vs. 7.7 +/- 1.1 ng/ml, p < 0.01) were elevated in the coronary sinus compared with aortic root in patients with UA. This was principally observed in those who were TnT positive. There was no cytokine gradient across the culprit plaque. CONCLUSIONS: There is an intracardiac inflammatory response in UA that appears to be the result of low-grade myocardial necrosis. The ruptured plaque does not appear to contribute to the acute phase response.     

Predictors and prognostic value of myocardial injury following stent implantation

BACKGROUND: Troponin I concentrations are frequently elevated following percutaneous coronary intervention (PCI) even in procedures without complications and are considered, by some, as predictive of long-term morbidity and mortality. We assessed whether post-PCI troponin I concentrations bore any relationship to clinical, angiographic and in-laboratory minor adverse events indicative of myocardial injury and evaluated, in follow-up, whether these levels are useful as a predictive markers of adverse events. METHODS: Patients (n=147) who were scheduled for PCI for stent placement were prospectively studied. In-laboratory events recorded were protracted chest pain, electrocardiographic changes, slow flows, dissections and lateral branch affectation. Troponin I and creatinine kinase MB fraction (CK-MB) mass were measured at baseline and post-procedure. Mean clinical follow-up was for 10.4+/-3.6 months. RESULTS: During PCI, at least one adverse event occurred in 34% of patients and, in 38% of them, there was an elevation of troponin I as compared to 5.1% of those patients without any adverse event (relative risk=7.4; P<0.001). Elevation of troponin I concentrations occurred in 16.3% of all patients, 79.2% associated with an AE. CK-MB was elevated in 15.6% of patients. On multivariate analysis, protracted chest pain, lateral branch involvement and slow flow remained statistically significant in relation to post-procedure elevations of troponin I concentrations. Clinical follow-up showed a poorer prognosis in patients who had had elevated troponin I concentrations. CONCLUSIONS: In-laboratory adverse event predict elevated post-procedure troponin I concentrations which are associated with myocardial injury. These elevations, in turn, predict poorer medium-term clinical outcomes.     

Role of cardiac troponin T in the long-term risk stratification of patients undergoing percutaneous coronary intervention.

AIMS: To investigate the long-term prognostic significance of pre- and post-procedure troponin T (TnT) elevations in patients undergoing percutaneous coronary intervention (PCI). METHODS AND RESULTS: TnT and CK-MB were measured pre- and post-procedure in 212 patients undergoing PCI. Major adverse events (composite of death, myocardial infarction and revascularization) were ascertained 6 years later. Pre-procedural TnT was a significant independent predictor of time to major events (hazard ratio [HR] 1.75, 95% confidence interval [CI] 1.16-2.64) and death or myocardial infarction. Post-procedural TnT elevation above normal was the only independent predictor of the primary end-point at 1 year (HR 2.39, 95% CI 1.09-5.26) but was not significantly related to event-free survival throughout follow-up. Post-PCI elevation of TnT 5x above normal, however, did significantly predict time to events during the entirety of follow-up. By contrast, CK-MB was not an independent predictor in any of the analyses. CONCLUSIONS: Our study confirms the long-term prognostic value of pre-procedural TnT elevation in patients undergoing PCI, and demonstrates the superior predictive ability of a post-procedural increase in TnT 5x normal for long-term adverse events. Whether the prognostic significance of smaller post-procedural TnT elevations extends beyond the intermediate-term awaits further investigation.     

The Erlanger chest pain evaluation protocol: a one-year experience with serial 12-lead ECG monitoring,two-hour delta serum marker measurements,and selective nuclear stress testing to identify and exclude acute coronary syndromes

STUDY OBJECTIVE: We determine the overall use of a 6-step accelerated chest pain protocol to identify and exclude acute coronary syndrome (ACS) and to confirm previous findings of the use of serial 12-lead ECG monitoring (SECG) in conjunction with 2-hour delta serum marker measurements to identify and exclude acute myocardial infarction (AMI). METHODS: A prospective observational study was conducted over a 1-year period from January 1, 1999, through December 31, 1999, in 2,074 consecutive patients with chest pain who underwent our accelerated evaluation protocol, which includes 2-hour delta serum marker determinations in conjunction with automated SECG for the early identification and exclusion of AMI and selective nuclear stress testing for identification and exclusion of ACS. In patients not undergoing emergency reperfusion therapy, physician judgment was used to determine patient disposition at the completion of the 2-hour evaluation period: admit for ACS, discharge or admit for non-ACS condition, or immediate emergency department nuclear stress scan for possible ACS. A positive protocol was defined as a positive result in 1 or more of the 6 incremental steps in our chest pain evaluation protocol: (1) initial ECG diagnostic of acute injury or reciprocal injury; (2) baseline creatine kinase (CK)-MB level of 10 ng/mL or greater and index of 5% or greater or cardiac troponin I level of 2 ng/mL or greater; (3) new/evolving injury or new/evolving ischemia on SECG; (4) increase in CK-MB level of +1.5 ng/mL or greater or cardiac troponin I level of +0.2 ng/mL or greater in 2 hours; (5) clinical diagnosis of ACS despite a negative 2-hour evaluation; and (6) reversible perfusion defect on stress scan compared with on resting scan. All patients were followed up for 30-day ACS, which was defined as myocardial infarction (MI), percutaneous coronary intervention/coronary artery bypass grafting, coronary arteriography revealing stenosis of major coronary artery of 70% or greater not amenable to percutaneous coronary intervention/coronary artery bypass grafting, life-threatening complication, or cardiac death within 30 days of ED presentation. RESULTS: Discharge diagnosis in the 2,074 study patients consisted of 179 (8.6%) patients with AMI, 26 (1.3%) patients with recent AMI (decreasing curve of CK-MB), and 327 (15.8%) patients with 30-day ACS. At 2 hours, sensitivity and specificity for MI (AMI or recent AMI) of SECG plus delta serum marker measurements was 93.2% and 93.9%, respectively (positive likelihood ratio 15.3; negative likelihood ratio 0.07). At the completion of the full ED evaluation protocol (positive result in >or=1 of the 6 incremental steps), sensitivity and specificity for 30-day ACS was 99.1% and 87.4%, respectively (positive likelihood ratio 7.9; negative likelihood ratio 0.01). CONCLUSION: An accelerated chest pain evaluation strategy consisting of SECG, 2-hour delta serum marker measurements, and selective nuclear stress testing in conjunction with physician judgment identifies and excludes MI and 30-day ACS during the initial evaluation of patients with chest pain.     

Impact of statin therapy on coronary intervention for non-ST elevation acute coronary syndrome with decreased low-density lipoprotein cholesterol

OBJECTIVES: The benefits of treating patients with acute coronary syndrome (ACS) with statins are well established. This study investigated the effects of statins on patients who presented with low levels of low-density lipoprotein (LDL) cholesterol, were diagnosed with non-ST elevation ACS, and subsequently underwent percutaneous coronary interventions (PCI). METHODS: From 2000 to 2003, 87 patients(mean age 68 +/- 10 years, 69 males, 18 females) underwent PCI because of non-ST elevation ACS, and had low LDL cholesterol on presentation. These patients were divided into two groups: those who had been taking statins (S-group, n = 46), and those not taking statins, or controls (C-group, n = 41). Only patients whose LDL cholesterol was < 100 mg/dl at admission (average: 82 +/- 12 mg/dl) were included in the study. Troponin-T (TnT), creatine kinase (CK), CK-MB, and high-sense C reactive protein (hs-CRP) were measured before and 6 hr after PCI. The two groups were evaluated at 6 months clinical follow-up. RESULTS: There was no difference in these markers before PCI in both groups. TnT and CK-MB in the S-group at 6 hr post-PCI were significantly decreased compared to those of the C-group (0.45 +/- 1.34 vs 1.40 +/- 2.37 ng/ml, respectively, for TnT, p = 0.04; 17.2 +/- 45.5 vs 81.3 +/- 157.2 IU/l, respectively, for CK-MB, p = 0.02). Major adverse cardiac events (MACE) defined as death, myocardial infarction, congestive heart failure and target lesion revascularization were evaluated after 6 months. There was no difference in MACE between the two groups. CONCLUSIONS: Statin treatment before PCI in patients with non-ST elevation ACS demonstrated beneficial effects such as less myocardial damage, even though both groups presented with low LDL cholesterol levels. However, no significant effect on MACE was seen at 6 months after PCI.     

Difference in elevation of N-terminal pro-BNP and conventional cardiac markers between patients with ST elevation vs non-ST elevation acute coronary syndrome.

BACKGROUND: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is elevated in patients with acute coronary syndrome (ACS), and is a powerful predictor of long-term mortality. Differences in the clinical utility and pathophysiological implication of NT-proBNP and conventional cardiac markers in patients with ST elevation (STE) vs non-STE (NSTE) ACS were investigated in the present study. METHODS AND RESULTS: Ninety consecutive patients admitted with acute chest pain and a diagnosis of unstable angina or acute myocardial infarction were analyzed. Patients with >or=Killip class II were excluded to focus on the effect of myocardial ischemia on the release of cardiac markers. The markers were measured on admission and analyzed according to the time from onset. Conventional cytosolic marker (creatine kinase-MB) and myofibril marker (troponin T: TnT) were both significantly higher in STE-ACS patients compared with NSTE-ACS patients. Conversely, NT-proBNP was significantly higher in NSTE-ACS patients than STE-ACS especially within 3 h of onset, suggesting a larger ischemic insult despite the smaller extent of myocardial necrosis compared with STE-ACS patients. There was no significant correlation between NT-proBNP level and left ventricular ejection fraction (LVEF) obtained at acute-phase echocardiography in either NSTE-ACS patients (LVEF 57.7+/-11.2%) or STE-ACS patients (LVEF 55.1+/-12.7%). Comparison between NT-proBNP and TnT levels revealed a marked difference of elevations, with significantly augmented elevation of NT-proBNP (p<0.001) in NSTE-ACS patients as compared with prominent elevation of TnT in STE-ACS patients. CONCLUSIONS: NT-proBNP is an early sensitive marker of myocardial ischemia that rises much higher in the earlier phase as compared with conventional markers of myocardial damage, especially in NSTE-ACS patients.     

Isolated elevation in troponin T after percutaneous coronary intervention is associated with higher long-term mortality.

OBJECTIVES: The aim of this study was to evaluate whether, in patients with normal post-procedure CK-MB, an isolated elevation in cardiac troponin T (cTnT) predicts long-term survival. BACKGROUND: Cardiac troponin T is a sensitive and specific marker of myonecrosis. There is little known about the incidence and prognostic significance of an isolated elevation of cTnT without a rise in creatine kinase (CK)-MB following PCI. METHODS: We evaluated the outcomes of 1,949 patients from the Mayo Clinic registry who had normal pre-procedure cTnT and CK-MB, required nonemergency percutaneous coronary intervention (PCI), and had normal CK-MB after the procedure. RESULTS: An elevation in cTnT (cTnT+) was observed in 383 patients (19.6%) (median 0.04 ng/ml, interquartile range 0.03 to 0.06 ng/ml). The TnT+ status was associated with adverse clinical and angiographic characteristics, and multivessel PCI. Over the median follow-up duration of 26 months, mortality (p < 0.001) and the combined rate of death and myocardial infarction (p = 0.004) were significantly higher in cTnT+ patients. Estimated 3-year survival for those with and without cTnT elevation was 86.9% and 93.2%, respectively. By multivariate analysis, an elevation in cTnT after PCI was an independent predictor of increased long-term mortality. A doubling in the post-PCI cTnT was associated with a partial hazard ratio of 1.20 (95% confidence interval 1.02 to 1.40; p = 0.023). CONCLUSIONS: An isolated minor elevation in cTnT after PCI provides long-term prognostic information regarding mortality and myocardial infarction.